Table 3 Negated sentences for Alzheimer's disease
From: BioN∅T: A searchable database of biomedical negated sentences
Gene | Sentence |
|---|---|
ACE | However these findings have not been confirmed by other reports (2,5,15,18,20). Among Italian studies, <negation>no association has been reported between ACE I/D polymorphism</negation> and AD (14,18,20), even if Palumbo et al. showed an increased frequency of D allele in subjects with cognitive impairment (14). In the present study, we investigated the role of ACE I/D polymorphism in a group of sAD patients. |
CH25H | From our results we conclude that the functional SNPs within LIPA and FLJ22476 are not associated with AD and therefore are not involved in pathogenetic mechanism leading to AD. Our data further do not support a relevant implication of both CH25H promoter polymorphisms and AD. |
CST3 | There was no interaction between CST3 with age or APOE. Our findings do not support a role of CST3 gene in Italian sporadic AD. |
GAB2 | Next, we explored GAB2 rs2373115 SNP singlelocus association using different genetic models and comparing AD versus controls or NNE controls. No evidence of association with AD was observed for this GAB2 marker (p > 0.17). To evaluate GAB2-APOE genegene interactions, we stratified our series according to APOE genotype and case-control status, in accordance with the original studies. |
MAPT | CONCLUSIONS: No evidence was found for an association of the non-synonymous polymorphism (Q7R) in STH and Alzheimer's disease. This finding is in line with earlier studies showing no association between MAPT and Alzheimer 's disease. |
PRNP | No significant association was found for the PRNP polymorphism in AD compared to controls either in Probable or in Definite AD series even after stratification for APOE polymorphism. This study does not support a role of PRNP polymorphism as a susceptibility factor for AD. |
SORL1 | Testing for association using dense SNPs in the SORL1 gene did not reveal significant association with AD, or with cognitive function when adjusting for multiple testing. In conclusion, our data do not support the hypothesis that genetic variants in SORL1 are related to the risk of AD. |
TF | No linkage disequilibrium between the BCHE K and TF C2 was observed either in both the AD patients and controls (P > 0.1). In conclusion, neither the BCHE K nor the TF C2 confers a risk for AD. |